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Facial Reanimation Surgery
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Demetrius Evriviades, Nicholas White
Seddon1 described the following types of neuronal injury: Neuropraxia. This is temporary cessation of conduction of the nerve with no loss of axon continuity. Neuropraxia is a transient phenomenon with complete recovery once the causative factor is removed. Axonotmesis. Damage is sustained to the axon resulting in Wallerian degeneration. Regeneration occurs at a rate of 1–4 mm a day and recovery is usually satisfactory.Neurotmesis. The nerve fibre is severed and the endoneurium disrupted. Recovery is unlikely.1, 2
The Facial Nerve and its Non-Neoplastic Disorders
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Christopher Skilbeck, Susan Standring, Michael Gleeson
The electrical impulse can only stimulate normal or neurapraxic fibres and cannot distinguish whether the remaining fibres are in a state of axonotmesis or neurotmesis. Thus, it cannot distinguish between injuries which have different prognoses.
Answers
Published in Thomas Hester, Iain MacGarrow, Surgical SBAs for Finals with Explanatory Answers, 2018
There are three main types of nerve injury: Neuropraxia – damage to the nerve fibres, in which there is no disruption of the nerve or its sheath. The conduction is interrupted for only a short period of time, with recovery commencing soon after the injury and is complete in 6–8 weeks.Axonotmesis – this is injury to the axon and myelin sheath without disruption of the continuity of its perineural sheath. The axon distal to the lesion degenerates, termed Wallerian degeneration, and this usually begins 24 hours after injury. The axonal skeleton disintegrates and the axonal membrane breaks apart; this is followed by degradation of the myelin sheath and macrophage infiltration. Regrowth in the axon occurs from the node of Ranvier proximal to the injury. The rate of regeneration is approximately 1 mm day−1.Neurotmesis – complete disruption of the nerve and nerve sheath. If the two ends are not too far displaced then regeneration may take place, however functional recovery will be incomplete.
Effect of Local and Systemic Dimethylsulfoxide on Peripheral Nerve Repair: A Controlled Randomized Experimental Study
Published in Journal of Investigative Surgery, 2021
Elif Sanli, Gungor Cagdas Dincel, Ebru Umay
Both DMSO groups showed higher PPT and TST results than the sham group at the end of the study. Functional recovery after an axonotmesis involves not only the number of regenerated axons but also the correct guidance of the axons toward their appropriate targets [32]. The functional tests also demonstrated that local or systemic administration of DMSO increases the rate of functional axonal regeneration. However, DMSO is more effective when applied locally. Clinical studies have demonstrated that high-dose systemic DMSO produces various adverse effects, such as nausea, vomiting, flushing, fever, chills, dyspnea, cardiac symptoms, transient hypertension, hypotension, anaphylaxis, encephalopathy, amnesia, and seizures [33]. Therefore, local administration of the drug may be better than systemic use.
Current concepts review: peripheral neuropathies of the shoulder in the young athlete
Published in The Physician and Sportsmedicine, 2020
Tamara S. John, Felicity Fishman, Melinda S. Sharkey, Cordelia W. Carter
Peripheral neuropathies of the shoulder and upper extremity in the young athletic population – older children, adolescents and young adults – are uncommon, yet may result in significant pain and impairment. It is therefore important to understand the relevant anatomy, common injury mechanisms, characteristic clinical presentation, pertinent physical examination findings, diagnostic tools, treatment options and functional outcomes for these injuries. Furthermore, familiarity with standard terminology for nerve injuries is essential. Neuropraxia is the mildest nerve injury type, in which the nerve structure and its primary elements remain intact, but the myelin sheath is disrupted. The cause of a neurapraxia is typically a stretch mechanism and neurapraxias are often associated with complete functional recovery. Axonotmesis is a nerve injury in which the axon itself is disrupted in addition to its myelin sheath, although the endoneurial tubes and supportive tissues (perineurium, epineurium) remain intact. The mechanism of axonotmesis is typically a more severe stretch or crushing-type injury of the neural tissue. Finally, neurotmesis is the most severe form of nerve injury, in which there is complete nerve disruption. Neurotmetic injuries have the least potential for recovery. Fortunately, most sports-related peripheral neuropathies are either neurapraxic or axonotmetic in nature, rather than fully neurotmetic.
Differential diagnosis of knee pain following a surgically induced lumbosacral plexus stretch injury. A case report
Published in Physiotherapy Theory and Practice, 2019
William R. VanWye, Harvey W. Wallmann, Elizabeth S. Norris, Karen E. Furgal
Interestingly, peripheral nerve, which is uniquely complex tissue, is the only soft tissue that does not follow the classic physiological phases of healing (Bélanger, 2015). Seddon classified peripheral nerve injury into 3 degrees of injury. The least severe is neurapraxia, followed by axonotmesis, and finally, the most severe form, neurotmesis (Burnett and Zager, 2004). Neurapraxia is a functional injury meaning there is focal demyelination, which is transient in nature. Axonotmesis and neurotmesis are not only functional, but also anatomical, which entails a disruption of nerve continuity (Burnett and Zager, 2004). A neurapraxia can range from 1 day to 3 months with full recovery expected. Axonotmesis has the most variability in recovery time and prognosis. Sunderland further divides axonotmesis into three classifications (i.e. Sunderland II–IV). In Sunderland II axonotmesis, the axon is injured, but the endoneurial tube is normal. This generally results in full recovery in 1–6 months. In Sunderland III axonotmesis, the endoneurial tube is injured; in this case, the recovery is less certain with partial return expected in 12–24 months. Lastly, with the Sunderland IV axonotmesis, only the epineurium is intact (i.e. the outer layer of the nerve) and recovery requires surgical intervention. Neurotmesis is a loss of nerve continuity, requiring surgical intervention with unpredictable recovery (Goubier and Teboul, 2015). Considering the patient’s steady progress and full recovery, the stretch injury appeared to be consistent with either a neurapraxia or Sunderland II axonotmesis.